Module 1: Incidence and prevalence Flashcards

1
Q

PECOT

A
  • Population: group of people who share a
    specified common factor.
  • Exposure group
  • Comparison group
  • Outcomes:
    • EGO: occurrence of dis-ease in exposure
    group.
    • CGO: occurrence of dis-ease in comparison
    group.
  • An average can be taken and EG
    compared to CG.
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2
Q

Incidence

A
  • Incidence: counting the number of onsets of disease events occurring during a period of time.
    • Longitudinal measure producing a rate.
    • Most appropriate for observable events.
    • Require dis-ease outcome to be categorical
    variable.
    • Measuring prevalence at two points of time
    and calculating the change in prevalence bt/
    the two points in time is a measure of the
    incidence of dis-ease over the period bt/ the
    two time points

ADVANTAGES
- Most useful for measuring causes of dis-ease
occurrence.
- Incidence is determined only by the dis-ease
risk in the population.
- Measures of incidence include events,
population and time.

DISADVANTAGES
- Incidence can be difficult to measure as one has
to observe events over time.

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3
Q

Prevalence

A

Prevalence: counting the number of people w/ a
dis-ease at a point in time.
• Cross sectional measure producing a figure.
• Most appropriate when transition from a nondis-eased state to a dis-eased state cannot
easily be observed and counted.

ADVANTAGES
- Prevalence is relatively easy to measure, as it is
static, taken for one point in time.
- Useful to funders and planners of health.

DISADVANTAGES
- Prevalence measures only include events and
population.
- Prevalence is determined by incidence, death
rate and cure rate

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4
Q

Prevalence

A

POINT PREVALENCE
- Point prevalence: outcome does not take any
previous time period into account and is simply
measured at one point in time.

PERIOD PREVALENCE
- Period prevalence: outcome/numerator depends
on the time period specified.
• Dis-ease outcomes cannot easily be
measured at one point in time, so we look
back and measure them over a period of
time.

A population could have a high incidence/low
prevalence if death/cure rate is also high.
A population could have a low incidence/high
prevalence if death/cure rate is also low.

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5
Q

C o m p a r i s o n s — R i s k

Differences and Relative Risk

A
  • Differences bt/ EGO and CGO can provide
    insight into the size of the effect of the study
    exposure on the dis-ease outcome.
  • Comparisons of dis-ease occurrence typically
    called ‘estimates of effect/association’ of an
    exposure on a dis-ease outcome.
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6
Q

RISK DIFFERENCE

A
  • EGO-CGO
  • Units — same unit as EGO/CGO calculation e.g.
    per x people over y years — more info.
  • Risk ratio can be the same whereas risk
    difference can be much smaller/larger.
  • Also called difference in occurrences, absolute
    risk (difference).
  • RD=0, no difference in effect of E and C on the
    study outcome.
  • Risk difference is an absolute risk reduction if
    risk is lower in the exposure group or an
    absolute risk increase if the risk is higher in the
    exposure group.
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7
Q

RELATIVE RISK

A
  • EGO/CGO
  • Also called risk ratio, relative risk difference,
    ratio of occurrence.
  • No units — less information.
  • RR=1, ‘no-effect’ value.
  • If dis-ease occurrence measures are calculated
    as averages, relative comparison of two mean
    scores is ‘relative mean’ (RM).
  • Relative risk reduction: relative risk is subtracted
    from 1.0, then expressed as a percentage.
  • Relative risk increase: 1.0 subtracted from
    relative risk, then express as percentage.
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8
Q

Non Random Error

A
  • Also called biases/systematic errors.
  • If error occurs because of poor study design,
    processes or measurement.
    • Valid study: small amount of random/nonrandom error.
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9
Q

RECRUITMENT -RAMBOMAN

A
  • Are participants representative sample from a
    defined population?
  • Described as external validity error, as when
    present findings may not be applicable to wider
    population.
  • Particularly important when major objective of
    study to measure characteristics of real population but participants recruited not
    representative of eligibles.

Selection bias: participants allocated to EG
different source to participants allocated to CG.
• Confounding error caused by allocation
process.
- Non response bias: non-responders different to
responders. Consider response rate.

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10
Q

ALLOCATION

A

How well were participants allocated to EG and
CG?
- Confounders: EG and CG differ in ways other
than allocation, and these other difference have
an effect on the study outcome.

  • RCTs: allocation by random process; all
    participants have equal chance of allocation to
    EG or CG, so groups are similar.
    • RCTs are known as experiments, because
    investigators actively control allocation
    process.
    • RCTs best way to stop confounding.
  • Complete baseline comparison to ensure
    RCTs w/ small samples don’t have different
    groups just through chance alone
 Concealment of allocation stops tampering
w/ randomisation process.
- Observational studies: allocate by measurement
and assign to EG and CG accordingly.
• People may lie/under-report to hide
embarrassment or they can’t remember.
- Avoid by good questionnaire design.
• Inaccurate measurement of exposure:
(allocation) measurement error.
• CG and EG often quite different: confounders
if study outcome influenced.
- Adjust for in analyses.
- Sufficient information must be collected
about other differences for adjustment
purposes.
- Confounding present in almost every
observational study.
• Two or more effects mix, all
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11
Q

MAINTENANCE

A

Will the validity of the study results be affected
by how well they were maintained in EG and
CG?
- Maintenance error: some participants’ exposure
status changes, or some are lost to follow-up.

• Did participants remain in their allocated
groups? Did they maintain their initial
exposure/comparison exposure?
- Long term cohort studies prone to maintenance
bias — offset by regular follow-ups.
- Maintenance not a problem for cross-sectional
studies.

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12
Q

BLIND AND OBJECTIVE MEASUREMENT

A

• Reduce error by blinding participants and
investigators to knowledge of which
intervention participants received.
• Blinding of outcome measurement ideal for
death certification when pathologist blind.
• R e d u c e e r r o r b y t a k i n g o b j e c t i v e
measurements where possible e.g. using a
machine.
- Measurement: use a standard definition.

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13
Q

ANALYSES

A
  • Confounding can be reduced by dividing
    participants into strata — stratified analysis e.g.
    age standardisation.
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14
Q

Random Error

A
  • Due to chance.
  • No single study will ever measure the exact truth
    in the whole population, even if it is a perfect
    study.
    • Every study an ‘estimate of the truth’.
    • Identical studies will produce different results.
  • All measures of EGO/CGO/RR/RD/NNT have
    random error.
    • Most random errors can be reduced by
    i n c re a s i n g s a m p l e s i z e , re p e a t i n g
    measurements.
  • Extreme events are often chance events:
    repeating measurements or studies w/ extreme
    results many times usually gives less extreme
    results — regression to the mean.
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15
Q

RANDOM SAMPLING ERROR

A
  • Inherent in every study.
    • N o s a m p l e w i l l e v e r b e p e r f e c t l y
    representative of the population.
  • Every sample will differ due to chance, and
    never include participants w/ identical
    characteristics.
  • Bigger sample, smaller differences bt/ sample
    and population
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16
Q

RANDOM MEASUREMENT/ASSESSMENT ERROR

A
  • R a n d o m m e a s u r e m e n t e r r o r e ff e c t s
    measurement of both exposures and outcomes.
  • Ability to measure biological factors the same
    way every time is often poor, particularly when a
    human operator is involved.
    • Avoid by repeated measurements w/ an
    average, or use, automatic, objective
    machine.
  • Randomness inherent in biological phenomena.
    • Inherent variability in biological phenomena,
    and therefore in its measurement.
    • Identical measurements of exposures and
    outcomes in the same or similar people can
    change from moment to moment.
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17
Q

RANDOM ALLOCATION ERROR

A
  • Groups in an RCT may differ by chance alone,
    particularly if trial is small.
  • Reduce by undertaking a larger study.
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18
Q

CONFIDENCE INTERVALS

A
  • Every epidemiological measure has random
    error in the estimate of the truth (EGO, CGO, RR,
    RD) in the population that the study participants
    were recruited from which can be estimated by a
    confidence interval.
  • 95% CI definition: in 100 identical studies using
    samples from the same population, 95/100 of
    the 95% CIs will include the true value for the
    population.
    • There is about a 95% chance that the true
    value in the population from which the
    participants were recruited lies within the
    95% CI, assuming no random error.
    • Bigger the study, narrower the CI.
  • As number of events in study increases, recruited. Probably no statistically significant difference
    • 95% CIs for RR and RD usually cross no effect line.
    • Study results not statistically significant.
    • If 95% CIs of RR and RD cross no effect line,
    best stated as too much random error to
    determine if there is a difference bt/ EGO and
    CGO, as opposed to stating there is no
    statistically significant difference.
  • 95% CI just touches no-effect line, study
    “borderline statistically significant” (compare w/
    statistically/not statistically significant).
  • Statistically significant event may be clinically
    significant if a clinician would make a similar
    decision whether the true result was near one
    end of the confidence interval or the other.
    Similarly, a small but statistically significant
    effect w/ a narrow confidence interval may not
    be of clinical significance.
    width of 95% CIs decrease.
    • Wider the interval, more random error in
    measure.
    • 95% CI most common for epidemiological
    studies.
    • 99% CI wider than a 95% CI.
    • Confidence limit: each end of CI.
  • If no overlap of confidence intervals, reasonable
    to assume that EGO and CGO are truly different
    from each other in the underlying population.
    • When there is no overlap of CIs in EGO and
    CGO, confidence intervals for RD and RR will
    not cross no-effect line.
    • Therefore measures of association bt/ EGO
    and CGO show real effect and ‘study results
    are statistically significant’.
  • If overlap of CIs, study unable to determine if
    EGO is different from CGO in the population
    from which the study participants were
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19
Q

META ANALYSES

A

Meta-analysis: analytical technique use to
combine results of studies mathematically to
generate a summary estimate of the effect. The
result could be statistically significant.
- Next best thing to a large study and reduces
random error in effect estimates.
• Does not reduce non-random error.
- Most studies too small to produce precise
estimates (i.e. w/ low random error) of disease
frequency therefore measures of association
also generally imprecise.
- Point estimates for different studies all show a
RR difference, but the 95% CIs cross the no
effect line.
• Conventionally, none of the trials are
statistically significant.
• Does not necessarily mean treatment not
beneficial, as studies could simply have been
too small.
• Studies must have low levels of bias (nonrandom error) and reasonably similar findings.
• Combining multiple similar studies in a metaanalysis is an alternative to conducting one
large study.
- Meta-analyses commonly undertaken to
combine results of multiple RCTs which
individually have too much random error to
demonstrate whether or not intervention
has a real effect.
• Ideal meta-analyses combine studies from
systematic reviews, however meta-analyses
can be taken of a non-systematically
recruited group of studies, although one
should be wary of the latter.

20
Q
A
21
Q
A
22
Q

Dahlgren and Whitehead and Causes of the causes

A

DETERMINANTS FOR INDIVIDUALS
- Any event, characteristic or other definable entity that brings about a change for better or worse
in health.
• Age, sex, ethnicity
• Water, shelter, sanitation (basic survival)
• Income, occupation, employment, education (provides opportunities for housing etc.)
• Housing, housing tenure, overcrowding, neighbourhoods (design of urban environments, is
one supportive and supported?, social and built environments)
• Access
• Deprivation
• Societal characteristics e.g. racism, attitudes to alcohol or violence, value on children (social
norms)
• Unconscious bias — racism, bullying, harassment
• Autonomy and empowerment — social cohesion (attitudes, resilience)
- What causes people to engage in activity which is a risk/protective factor — determinant of
determinant.

23
Q

DETERMINANTS AND THE LIFE COURSE

A
  • Determinants of health may vary at different life stages.
  • Three ways in which life course events can interact to influence long-term health and wellbeing:
    • Cumulative — notion of poverty trap, born into more or less wealth, children of parents of
    grandparents.
    • Multiplicative — multiplied effects on risk— multiple CVD risk factors combine to give
    fractional increase.
    • Programming — Barker hypothesis — genetics, in utero impacts critical periods in one’s
    development.
24
Q

DAHLGREN AND WHITEHEAD MODEL

A
Person — micro (individual)
- Non-modifiable genes and hereditary,
and individual lifestyle factors, e.g.
attitudes to smoking, alcohol, diet,
exercise, influenced by social and
community networks.

• Community — meso (family, living, work)
- Local influences such as home, workplace and neighbourhood (behaviour of family,
friends, groups like me, community and its makeup.), and wider societal levels such as
health and education.

• Environment — macro (national/global)
- Cultural, social, political, physical and built
environment.
- Shared beliefs, values, attitudes and culture of broad
groupings.
- Govt regulation and policy.

25
Q

Upstream and downstream

A

UPSTREAM VS DOWNSTREAM INTERVENTIONS
- Downstream interventions operate at a micro (proximal) level, including treatments systems,
and disease management.
- Upstream interventions operate at the macro (distal) level, such as government policies and
international trade agreements.

26
Q

PROXIMAL AND DISTAL DETERMINANTS

A

Proximal determinants of health near (directly and readily associated e.g. lifestyle and
behavioural factors) the change in health status.
- Distal determinants of health are either distant in time or place from the change in health status.
• Also referred to as upstream factors, e.g. national, political, legal and cultural factors that
indirectly influence health by acting on proximal factors.

27
Q

STRUCTURE AND AGENCY

A
  • Structure: social and physical environmental conditions/patterns (social determinants) which
    influence choices and available opportunities — upstream (three outer arches).
  • Agency (empowerment): capacity of an individual to act independently and make free choices
    — downstream (two inner arches).
28
Q

Māori health: HISTORY

A
  • Early contact
    • Māori initially flourished economically and
    socially.
    • Beginning of complex changes.
  • Official engagement
    • Colonisation, Declaration of Independence,
    Treaty of Waitangi, New Zealand.
    • Herald of an era of depopulation, disease and
    dispossession.
  • Colonisation
    • Not value-free.
    • Assumptions held by colonisers.
    • Notions of superior and inferior peoples.
    • Notions of civilisation especially religious but
    also economic and scientific e.g. land use,
    conservation.
    • Notions of deserving and undeserving.
  • Societal barriers still obvious today.
29
Q

IMPLICATIONS OF TREATY

A
Creation of Government — Article I
• Construction of state sector — justice system,
education, health, welfare etc.
• Constitution Act 1852 created settler
Government, determined voting rights
- Laws and policies — Article II
• Disregard for Māori voice/authority despite
Article II
- Māori land — historical basis of settler wealth
• Pre-emption clause of Treaty
- Māori land court — 1860s
- Individual title
- Different or denied citizenship — Article III
• Old-age pensions 1898
- Equal provisions for Māori and pakeha.
- Asian excluded.
- Māori access difficult — through Māori land
court.
- Māori regularly removed from rolls.
- Reduced amount paid to Māori.
• Social Security Act 1938
- Underpayment continued after WWII.
30
Q

RELATIONSHIP OF TREATY TO HEALTH

A
  • Policy alienation.
  • Land alienation:
    • Social disruption of community.
    • Breakdown of political power and alliances.
    • Economic resource depletion and poverty.
    • Resentment by indigenous peoples.
  • Unequal (inferior) citizenship:
    • Entrenchment of poverty and dependance.
    • Increased barriers to development.
    • Acceptance of inequity by non-indigenous
    groups.
    • Resentment, frustration and anger.
    • Social breakdown, crime, high risk behaviours.
31
Q

Prevention, promotion, protection: approaches to

taking action

A

Population-based (mass) strategy
- Whole population.
- Reduce health-risks/improve outcome for all individuals of
population.
- Useful for common disease/widespread cause.
• Immunisations, seatbelts, low salt foods in supermarkets.
ADVANTAGES
- Radical, addressing underlying causes.
- Large potential benefit for whole population.
- Behaviourally appropriate — change social norms; something becomes acceptable.
DISADVANTAGES
- Small individual benefit.
- Poor individual motivation.
- Whole population exposed to downside of strategy (less favourable benefit to risk ratio).

32
Q

High-risk individual strategy

A
  • Focuses on perceived high-risk individuals.
  • Well matched to individuals and their concerns.
    • Obese adult interventions, intravenous drug users (NZ Needle Exchange), high systolic BP
    individuals.

ADVANTAGES

  • Tailored and targeted; appropriate to individuals.
  • Individual motivation.
  • Cost-effective use of resources.
  • Favorable benefit to risk ratio.

DISADVANTAGES

  • Cost of screening; need to identify individuals, and
  • Temporary effect (e.g. breast screening cohort).
  • Limited potential (small sample size).
  • Behaviourally (culturally) inappropriate.
33
Q

Health Promotion

A

Acts on determinants of wellbeing.
- Positive, health/wellbeing focus.
- Enables/empowers people to increase control over
— and improve — their health.
- Involves whole population in everyday contexts.
- Primary-care orientated.

34
Q

OTTAWA CHARTER FOR HEALTH PROMOTION (WHO

A

21 November 1986.
- First International Conference on Health Promotion.
- ‘Mobilise action for community development’.
- Health is:
• A fundamental right for everybody.
• Requires individual and collective responsibility.
• Opportunity to have good health should be equally available.
• Good health is an essential element of social and economic
development.
- Three basic strategies:
• Enable — individual
- Provide opportunities for all individuals to make healthy choices through access to
information, life skills and supportive environments.
• Advocate — systems
- Create favourable political, economic, social, cultural and physical environments by
promoting/advocating for health and focusing on achieving equity in health.
• Mediate — individuals, groups and systems
- Facilitate/bring together individuals, groups and parties w/ opposing interests to work
together and compromise for health promotion.
- Five priority action areas:
• Develop personal skills: life skills education, ICT for health, awareness campaigns.
• Strengthen community action (community empowerment): Self-help groups and community
organised services (e.g. HIV/AIDS), initiatives to promote healthy schools, cities etc.
• Create supportive environments: air control, water and sanitation, speed bumps, work safety.
• Reorient health services towards primary health care: care responsive to needs of patients/
families (considering culture, social norms, physical and mental capacities, healthcare skills,
aspirations, resources), healthcare education, amenities to enhance hospital experience.
• Build healthy public policy: Tax alcohol and cigarettes, seat-belt use, ban smoking in public
places, food and drug control, mandatory sports in schoo

35
Q

Disease Prevention

A

Disease focus.
- Looks at disease/injury and ways of preventing them.
- Primary: limit incidence by controlling specific causes and
risk factors e.g. seatbelts, immunisation.
- Secondary: reduce more serious consequences of disease e.g. hip fracture screening, lifeguard
services.
- Tertiary: reduce progress of complications of established disease: counselling services for
PTSD, rehabilitation for burns patients.

36
Q

Health Protection

A

Predominantly environmental hazard focused.
- Risk/hazard assessment e.g. environmental
epidemiology, biosecurity, safe air and water.
- Monitoring e.g. biomarkers of exposure to
hazardous substances.
- Risk communication e.g. relating environmental
risks to public.
- Occupational health e.g. workplace safety
regulations.

37
Q

Establishing causality in

population health

A

Association and causation
- Explore the concepts of association and causation in
understanding the determinants of health and
attempts to improve population health.

EPIDEMIOLOGY AND THE CAUSES OF DISEASE
- Epidemiology, causes of disease, appropriate
preventative measures can be introduced.
- Not determine disease cause in individual, but
relationship/association bt/ exposure—disease in
populations.
• Links exposures—outcomes.
• Lind’s controlled-trial of 12 sailors (small sample
size) showed citrus consumption associated w/
scurvy prevention.
- Preventative action taken before the cause
identified

38
Q

Bradford Hill and Rothman’s Criteria

A

BRADFORD HILL CRITERIA (1965)
- Establish causality. - Aid, not definitive checklist.
- Not all criteria needed to establish causality.
• Temporality.
- Essential.
- First cause then disease.
• Questionnaire to establish exposures then
deaths followed up.
• Strength of association.
- Stronger association, causality more likely, in
absence of known biases (selection,
information, confounding).
• Consistency of association.
- Replication of findings by different investigators,
different times, places, different methods.
• Biological gradient (dose-response).
- Incremental change in disease rates—
corresponding changes in exposure.
• Biological plausibility of association.
- Does the association make sense biologically?
• Specificity of association.
- Weakest criteria. - A cause leads to a single effect, although a
single cause often leads to multiple effects.
• Reversibility.
- Demonstration that under controlled conditions,
changing exposure causes a change in the
outcome.

39
Q

ROTHMAN’S CAUSAL PIES

A
  • A cause of a disease: event, condition, characteristic
    (or combination) playing essential role in producing
    disease.
    • Sufficient cause (causal mechanism): factor(s)
    inevitably producing specific disease.
    • Component cause: factor contributing to disease
    causation, not sufficient alone to cause disease.
    • Necessary cause: factor (component cause) must
    be present for disease to occur.
  • Use association/other factors to infer causation and
    intervene to prevent disease.
  • Can intervene at any point of pie.
  • Knowledge of complete pathway not prerequisite for
    introducing preventative measures.
  • Removing one of component causes can prevent
    disease.
40
Q

Screening: a special type
of prevention strategy
S u c c e s s f u l s c r e e n i n g
initiatives

A

SCREENING FUNDAMENTALS
- Screening: identifying risk factors for
disease/unrecognised disease by applying
tests, large scale to population.
- Can be primary (alcohol intake to prevent
breast cancer)/secondary (breast cancer
screening)/tertiary (screening for bone
density after breast cancer chemotherapy).

41
Q

SCREENING COMPONENTS

A
COMPONENTS
- Eligible population (most susceptible to
disease).
- Screening test: simple, cheap, easily
applied to many.
- Diagnostic test: best possible test for
testing disease presence.
- Intervention/treatment.
- Re-screening at given time interval.
42
Q

Diseases and screening tests

A
SCREENING CRITERIA
- Suitable disease:
• Important public health problem:
relatively common/relatively uncommon
but early detection and intervention leads
to better outcome.
• Knowledge natural history disease (or
relationship risk factors—condition).
- Detectable early (detectable risk factor/
disease marker).
- Increased pre-clinical phase duration
— screening more effective: more time
to screen, treat.
- Suitable test:
• Reliable (consistent results), safe, simple,
affordable, acceptable, accurate (test’s
ability, indicate which individuals have
disease/not).
- Accuracy: gold standard diagnostic
test, but can’t be applied to large
populations. Screening test judged
against diagnostic test, less expensive.
- Suitable treatment:
• Evidence early treatment->better
outcomes.
• Effective, acceptable, accessible
treatment.
• Evidence-based policies covering
eligibles for treatment/appropriate
treatment to be offered.
- Suitable screening programme:
• Benefits must outweigh harm.
• RCT evidence screening programme will
result in:
- Reduced mortality.
- Increased survival time.
• Lead time bias.
• Length time bias.
43
Q

Screening test performance

A

DEFINITIONS

  • True positive: disease, positive test.
  • False negative: disease, negative test.
  • False positive: no disease, positive test.
  • True negative: no disease, negative test.
44
Q

INTERPRETATIONS OF SENSITIVITY AND

SPECIFICITY

A
• Sensitivity high if proportion of true
positives high.
• Specificity high is proportion of true
negatives is high.
- Fixed characteristics of tests.
• In two equally sized populations w/
different prevalences of disease,
predictive values will be different.
45
Q

Prioritizing in public health prioritization

A
EVIDENCE-BASED MEASURES
- Descriptive:
• Consider current problem (outcomes),
who most/least affected (e.g. Treaty
obligations may prioritise one disease
over another, e.g. even though stroke
overall greater death rate, respiratory
disease rates greater for Māori
- Explanatory:
• What are determinants/risks? Why
getting worse/better? Why populations
different? Epidemiological measures used
in prioritisation e.g. determine major risk
factors of disease burden.
- Evaluative:
• What can improve health outcomes and
in whom? How well can problem be
solved?
- Target population, expected number in
population reached, evidence of
effectiveness (based on known
success rates), cost.
- Age at death/premature mortality —
years of potential life lost to death
(YLL).
- Time lived w/ disability — years lived
w/ disability (YLD).
- Population Attributable Risk.
• D o e s p r o b l e m / r i s k f a c t o r
disproportionately affect population sub
groups? Why? ToW considerations. 
• Economic feasibility: economic sense to
address problem/consequences of not
doing so?
• Opportunity cost: potential other health
benefits had money been spent on next
best alternative intervention/healthcare
programme.
• Acceptability: Will community/target
population accept problem being
addressed? Competing interests?
46
Q

Population Attributable Risk

A

ATTRIBUTABLE RISK
- RD=AR (EGO-CGO).
• EGO = incidence in exposed population.
- Amount of extra disease attributable to
particular risk factor in exposed group.

POPULATION ATTRIBUTABLE RISK
- Amount of extra disease attributable to
particular risk factor in particular population.
- If association causal, amount of disease
theoretically preventable if particular risk
factor removed from population.
- RR: Compared w/ non-smoking mothers,
smoking mothers are four times more likely
to have a pre-term baby

  • RD: Smoking mothers will have 600 more
    preterm babies per 1000 women than nonsmoking mothers.
  • PAR: For every 1000 mothers in population,
    we can prevent 90 preterm births by
    removing heroin addiction as a risk factor.
  • PAR higher when disease prevalence higher
    in population.